title: Prenatal programming of insulin secretion in intrauterine growth restriction.
abstract: Intrauterine growth restriction (IUGR) impairs insulin secretion in humans and in animal models of IUGR. Several underlying mechanisms have been implicated, including decreased expression of molecular regulators of β-cell mass and function, in some cases shown to be due to epigenetic changes initiated by an adverse fetal environment. Alterations in cell cycle progression contribute to loss of β-cell mass, whereas decreased islet vascularity and mitochondrial dysfunction impair β-cell function in IUGR rodents. Animal models of IUGR sharing similar insulin secretion outcomes as the IUGR human are allowing underlying mechanisms to be identified. This review will focus on models of uteroplacental insufficiency.
authors.affiliation: Robinson Institute, and School of Paediatrics and Reproductive Health, University of Adelaide, SA, Australia, USA. kathy.gatford@adelaide.edu.au
authors.forename: Kathryn L
authors.initials: KL
authors.lastname: Gatford
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Simmons
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000196:embryology / Q000235:genetics; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005317:Fetal Growth Retardation / Q000235:genetics* / Q000503:physiopathology; D005333:Fetus / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000502:physiology; D011247:Pregnancy
chemical_list: D007328:Insulin